Nikolaos Kokras1, Efthymia Papadopoulou2, Georgios Georgiopoulos2, Christina Dalla3, Ioannis Petropoulos2, Christos Kontogiannis2, Ageliki Laina2, Dimitrios Bampatsias2, Konstantinos Stellos4, Anastasios V Kouzoupis5, Kimon Stamatelopoulos6. 1. First Department of Psychiatry, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, Greece; Department of Pharmacology, Medical School, National and Kapodistrian University of Athens, Greece. 2. Department of Clinical Therapeutics, Vascular Laboratory, Alexandra Hospital, Medical School, National and Kapodistrian University of Athens, 80 Vas. Sofias Str, Athens 11528, Greece. 3. Department of Pharmacology, Medical School, National and Kapodistrian University of Athens, Greece. 4. Cardiovascular Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle Upon Tyne, UK; Cardiothoracic Centre, Newcastle upon Tyne Hospitals, NHS Foundation Trust, Newcastle upon Tyne, UK. 5. First Department of Psychiatry, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, Greece. 6. Department of Clinical Therapeutics, Vascular Laboratory, Alexandra Hospital, Medical School, National and Kapodistrian University of Athens, 80 Vas. Sofias Str, Athens 11528, Greece; Cardiovascular Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle Upon Tyne, UK. Electronic address: kstamatel@med.uoa.gr.
Abstract
BACKGROUND: Major depression is associated with endothelial dysfunction and arterial stiffening, which may mediate development of hypertension and increased cardiovascular risk. The effect of response to antidepressant treatment on these vascular parameters has not been elucidated. AIMS: We aimed to assess the net effect of antidepressant therapy on endothelial function and arterial stiffness in patients with psychotic depression. METHOD: Thirty-seven patients with major psychotic depression, according to DSM-IV-TR, were treated with titrated citalopram 20-60 mg and risperidone 0.5-1 mg and were followed for 6 months. Twelve additional patients who denied treatment, or were non-compliant, were also followed for the same time period. Vascular function was assessed by flow-mediated dilatation (FMD), carotid-femoral pulse wave velocity (PWV) and augmentation index (AI), at baseline and at the end of follow-up. RESULTS: Aortic and peripheral blood pressure (BP), PWV, FMD and AI (p < 0.05 for all) were significantly improved in the group that received treatment. Overall, only responders to treatment (n = 24) presented significant improvements in all hemodynamic and vascular parameters (p < 0.05 for all), irrespectively of traditional cardiovascular risk factors (TRFs), vasoactive medication and BP lowering. In a secondary analysis, patients with psychotic depression presented worse endothelial function as compared to controls matched for TRFs. LIMITATIONS: Non-randomized study. CONCLUSIONS: Patients who respond to therapy for major psychotic depression present sustained improvement in vascular function. Given that depressed patients are considered to be at high cardiovascular risk and are often non-compliant with treatment, further research to assess cardiovascular benefits of vigilant monitoring of antidepressant therapy is warranted.
BACKGROUND: Major depression is associated with endothelial dysfunction and arterial stiffening, which may mediate development of hypertension and increased cardiovascular risk. The effect of response to antidepressant treatment on these vascular parameters has not been elucidated. AIMS: We aimed to assess the net effect of antidepressant therapy on endothelial function and arterial stiffness in patients with psychotic depression. METHOD: Thirty-seven patients with major psychotic depression, according to DSM-IV-TR, were treated with titrated citalopram 20-60 mg and risperidone 0.5-1 mg and were followed for 6 months. Twelve additional patients who denied treatment, or were non-compliant, were also followed for the same time period. Vascular function was assessed by flow-mediated dilatation (FMD), carotid-femoral pulse wave velocity (PWV) and augmentation index (AI), at baseline and at the end of follow-up. RESULTS: Aortic and peripheral blood pressure (BP), PWV, FMD and AI (p < 0.05 for all) were significantly improved in the group that received treatment. Overall, only responders to treatment (n = 24) presented significant improvements in all hemodynamic and vascular parameters (p < 0.05 for all), irrespectively of traditional cardiovascular risk factors (TRFs), vasoactive medication and BP lowering. In a secondary analysis, patients with psychotic depression presented worse endothelial function as compared to controls matched for TRFs. LIMITATIONS: Non-randomized study. CONCLUSIONS:Patients who respond to therapy for major psychotic depression present sustained improvement in vascular function. Given that depressedpatients are considered to be at high cardiovascular risk and are often non-compliant with treatment, further research to assess cardiovascular benefits of vigilant monitoring of antidepressant therapy is warranted.
Authors: Gerwyn Morris; Basant K Puri; Lisa Olive; Andre Carvalho; Michael Berk; Ken Walder; Lise Tuset Gustad; Michael Maes Journal: BMC Med Date: 2020-10-19 Impact factor: 8.775